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Friday, May 31, 2019

Two people who read my column before it is published (my wife
and then my editor), have told me recently that the Very Low Carb diet that I
espouse is either “too hard” or “unpalatable” and not likely to be tried, especially by “newbies” who are
considering Low Carb as the way to go for a Lifestyle Change and Way of Eating.

My goal is good health outcomes: losing weight, feeling great,
and three critical and related health markers: blood glucose, blood lipids and
blood pressure. Through diet alone, or with minimum medications, patients can
avert or delay the onset, and treat and reverse conditions like Type 2
diabetics and Pre-diabetics, heart disease, stroke, many cancers, and even cognitive
impairment. Similar outcomes are seen by many people who follow this Lifestyle.

Improvements in the way you feel will manifest quickly when
you switch from being a sugar burner to a fat burner. You will see it in the
loss of hunger, in feeling full of energy instead of sleepy, in your elevated
mood, and in the lab reports that your doctor will see. Your doctor should also
be aware of the reductions in all-cause mortality and the co-morbidities of all
these diseases of Western civilization that are now widely reported in the
scientific literature.

Whether they know how you did it or not, your doctor will be
very happy for you. They won’t have
to cajole or hector you to change your ways. They’ll just look at the results –
the office scale, the blood pressure cuff, and your lab blood test reports and
smile. Then, they will say to you, “Just keep on doing what you are doing.”

Anyway, this is all preface to “then and now.” What my
“constructive critics” mean when they tell me I am being too zealous. My wife
says, “Not everyone is like you,” and my editor gags at the idea of eating a
can of sardines for lunch every day. Okay, I get it. But I didn’t start off
like that. I recall that when I first started eating Very Low Carb more than 17
years ago, I ate on average 50 grams of carbohydrate a day some weeks, and 1,800
or even 2,200 calories a day, and occasionally I binged. But I weighed 375 pounds,
and I was transitioning from a lifestyle of indulgence to a more disciplined
Way of Eating. But I still lost weight – about 2 pounds a week, in toto 170
pounds.

The amazing thing is that within a day or two of starting on
strict Atkins Induction (20 grams of carbs a day), I was getting “hypos” every
day, and I just had to eat a
candy bar (LOL). I called the doctor, and he first told me to stop taking one
of three oral meds. Then, the next day when the hypos continued, he ordered me
to cut the other two oral meds in half and then soon thereafter to cut them in
half again. A few years later, when I switched to Bernstein (30 grams of carbs
a day), I was able to drop one of the other two., continuing with just
Metformin. From the beginning of eating Very Low Carb, my blood sugars came
into control (which they were not
even on all three oral meds),
and my A1c dropped into the “non-diabetic” range, where it has remained now for
17 years.

So, the message is: You don’t have to be a fanatic to make
this Way of Eating work for you. In my opinion, it’s best if you go “all in”
because you get the benefit of not
being hungry. That’s because you will transition from getting your
energy from foodto
getting your energy from your body fat
stores. But start out wherever you can – say at 100 grams a day until you get used to it,
or maybe even 20 grams of
carbohydrates a meal.

Remember, the Recommended Daily Allowance (RDA) on the
Nutrition Facts panel on processed (boxed and bagged) foods is 300 grams of carbohydrate a day for women.
That’s 60% of your daily food intake on a 2,000 calorie a day diet, and most
people actually do eat between 55% and 60% of their calories from
carbohydrates.

Reducing that by two-thirds to 100g/day is a big step in itself. Then, after your body (and your conscious you) has acclimated, if you still haven’t met
your blood glucose or weight loss goals, cut them again to say 20 grams of carbs/meal. Eventually,
you may get to where I and my body am/are
happily now: +/- 15 grams of carbs a day.

Thursday, May 30, 2019

I have mused a few times about how most doctors and
dietitians, especially established practitioners, are in a bind. The younger
ones can still have an epiphany without ruining their practices. It must be a
rude awakening when they do, but they can do it with integrity if they are
truth seekers. The older ones, as I see it, have three problems:

1) The mantra when they were schooled in medicine (doctors)
and nutrition (dietitians) – never to be cross-fertilized – was the coda of the
day: the diet-heart hypothesis (the saturated fat/cholesterol/heart disease hypothesis)
from the now widely discredited work of Ancel Keyes. When he joined the Board
of the American Heart Association in 1961,, and made the cover of Time Magazine, the “die was cast.”
Everybody read Time in those days.
Now, it’s just a pamphlet! But the medium spread the message. To this day, the
health establishment trumpets it.

2) The specialties in medicine are governed by medical
associations that set “Standards of Practice” that are in turn adopted by
Medicare and then by private insurance companies. In some ways it makes medical
care simpler, quicker and certainly less risky. The older clinician gives you and
the standard exam, the standard reimbursable tests using the standard medical
codes, for which he gets paid, and the standard treatment: a script for pill(s)
and advice to lose weight (“eat a balanced diet”) and “move more” (exercise). Then,
you’re outta there. Next patient!

3) The problem is, how can a doctor deviate from this? Will
he get paid for that non-standard test? How can a doctor change when he has an
open mind and sees something that works after so many years of the exact
opposite? Admit that what he has been prescribing for many years, doesn’t work
that well? That what he has been telling you all these years is wrong? That it
is exactly backwards? That the diet-heart hypothesis was not evidence-based,
just bad science? Many doctors and scientists have said so, but what will the
patient think if his doctor,
his trusted personal health advisor, does a complete about face? How can I still
be confident? Is he a quack?

Many doctors and nutrition scientists are saying this now, but to be fair, not for the same
indications. My doctor, who was a board-certified internist and cardiologist,
suggested that I try Atkins Induction – off label, as it were – to lose weight. He had just read
Gary Taubes’s July 2002 New York Times
Sunday Magazine cover story, “What If It’s All Been a Big Fat Lie.” He had tried
it himself, had lost 17 pounds in a little over a month (with no ill effects on
his cholesterol panel), and suggested I try it. Ever cautious, though, he did monitor
me monthly for a year.

Anyway, most doctors would have a hard time doing what my
doctor did, even if they believed in it. But you, their patient, are not in the bind that they are in. You can be “fickle without
being feckless.” You’ve got
nothing but your improved health at stake (LOL). Not that that’s
inconsequential. You, the patient, can
change what you eat.

Okay, you don’t have to do “the full Monty” to start with, or
ever, for that matter. You could start with just a low carb, moderate protein
and high fat diet. That’s still a very big improvement over the way you are
probably eating now. The Recommended Daily Allowance (RDA) of the Standard
American Diet (SAD), the one on the Nutrition Fact Panel on packaged (boxed and
bagged) foods is 60% carbohydrate, 10% protein and 30% fat. You could do 40%
carb, 30% fat and 30% protein. That would be a reduction from 300 grams of
carbs to 200. Or, you could work your way down to 20% carbs (100 grams of carbs/day
on a 2,000kcal/day diet).

Then, after you adjust (and lose weight and lower your
triglycerides and raise your HDL), you could try 20 grams per meal, with no
snacks (you won’t have any cravings – in fact, you won’t even be hungry). Or, you could do Bernstein
(6-12-12 = 30/day), or Atkins Induction (20g/day) or my current Way of Eating.
I do 15g of carbs/day. I now eat 5 grams of carbs at breakfast, zero at lunch,
and 10 at supper, unless I have a glass or two of wine, which I often do now.
That bumps me up to between 25 and 30 grams of carbohydrate a day. And I’m still
ketogenic.

The point is: You
are not constrained by your profession. You
will not be feckless if you change the way you eat. You can be fickle. You
can try eating lower carb, or low carb, or very
low carb the way I do. It’s okay to do what works for you. It’s your
health. It’s your life. And
now, it’s your time to decide.

Wednesday, May 29, 2019

Your Mileage May Vary (YMMV) is an expression
that I didn’t put much stock in when I first read it years ago on a Low Carb
Forum. I was a neophyte in the self-management
of my Type 2 diabetes, even though I had been a Type 2 for 16 years. Up until
then, like most of us, I had left my health care in the hands of my physician.
So, in those early days of self-management – if I thought about it at all, I thought
that we Type 2s were all pretty much alike.

What prompted me to write about this [in 2013] was
a personal experience I had with my blood sugar (BS) control. My most recent
A1c was 5.6%. It’s been better and, of course, worse. I had been eating a
restricted-calorie, Very Low
Carb (+/-15g) ketogenic diet for several months to lose weight and had lost 25
pounds. Five consecutive daily fasting blood glucose readings averaged 90mg/dl,
with a tight range. Then, at a small dinner party in our home, I ‘blinked’ (transgressed):
I had about a cup of risotto (with Osso Bucco and broccoli rabe) and some dessert
(2 homemade cookies and 2 bouillon-cube sized petit fours). My body hadn’t had
this much starch and sugar in a long time, and it was not prepared for it. My fasting blood glucose the next
morning was 120mg/dl. The next day my FBS was still 117. The next day 114, the
next 123, and so on. I had fallen off the ketogenic cliff and had lost BS control.

That’s where YMMV comes in. It depends on your
medical history (both the type and degree of metabolic dysfunction and when and
how you and/or your doctor responded to the discovery that you were Pre-diabetic
or a diagnosed Type 2. I was diagnosed in 1986. The first thing my doctor did,
besides advising me to lose weight (“eat less on a ‘healthy’ balanced diet”), was to prescribe a sulfonylurea(SU), a class of
oral anti-diabetes medication that makes the pancreas produce more insulin. At
the time, sulfonylureas were the only
oral anti-diabetes medication prescribed in the U. S. When I continued
to eat carbohydrates, and the SU didn’t get my BS under control, my dose was
increased until I was ‘maxed-out’ on this med. Then, when Metformin was
approved for use in the U. S., I started on and eventually was maxed out on it too
and started on a 3rd oral med. On a “balanced” diet, however, my blood sugar continued to elude control,
and my Type 2 diabetes inexorably
progressed.

My Type 2 diabetes didn’t stop its progression until
I changed my diet. In fact, it reversed to the point of being undetectable as long as I “eat right”
(VLC). After starting to eat Very
Low Carb (VLC), in the first week I forced to take fewer and fewer oral anti-diabetic
meds. Still, it was almost five years before I completely titrated off the SU,
so I took an SU at some dosage level for 21 years. So, I wondered, what effect
did this have on my pancreas?

Well, I’m not a doctor, so I’ll refer instead to
what one of my favorite diabetes specialists, Ralph A. DeFronzo, M.D., has been
saying for years. In his Banting-award lecture at the 2008 Annual Meeting of
the American Diabetes Association in San Francisco, Dr. DeFronzo said, “By the
time that the diagnosis of Diabetes is made, the patient has lost over 80% of
his/her β-cell function.” He also said in the first paragraph of the full-text
article published by the ADA on the NIH website, “Sulfonylureas are not
recommended because, after an initial improvement in glycemic control, they are
associated with a progressive rise in A1c and a progressive loss of β-cell
function.”

So, where does this leave me? If I had lost over
80% of my β-cells upon being diagnosed, and continued eating a “balanced” diet (with
lots of carbs) for another 16
years, my pancreas still needed to make insulin with fewer β-cells. The SU continued
to push it to do that because the goal
was to control my blood sugar with medications.

So, a disease that starts with insulin resistance
progresses to pancreatic β-cell burnout as it responds to that resistance. That is inexorable if you don’t dramatically
change your diet. It will likely accelerate if you continue to use a sulfonylurea to get your pancreas
to pump insulin. That is the “course of action” of the disease. That course will
be inexorable if 1) you don’t
change your diet and 2) you don’t stop taking a sulfonylurea. You must
do both to protect and preserve what pancreatic β-cell function you
have left before it’s too late.
If you choose to do both 1)
and 2) when you are at an early stage
of this disease, YMMV from mine. If you don’t, like me, you may become
totally carbohydrate intolerant. And like me, you will not be able to “cheat” from time to time and get away with
it.

Tuesday, May 28, 2019

While floating down a “lazy river” at a resort in
Puerta Vallarta, Mexico, I began a conversation with another “floater.” I
turned the conversation to my interest in nutrition for Type 2 diabetics and
told my new “friend” what I had accomplished a few years before by eating Very Low
Carb. I followed Atkins induction (20g of carbs a day) for 9 months and lost 60
pounds. I then described how I had drifted away from VLC for a number of years.
It turns out my “friend” was one of those enlightened physicians (a Canadian)
who then bluntly exclaimed, “You’re in denial!”

He was right, of course. It’s easy to delude
oneself. We do it all the time, every day, in many ways. It’s called
rationalization, a process of reasoning, or suspension of reason, that allows
us to do something that we know is a “bad” option. It’s a lack of
self-awareness. The process is invidious. It sneaks up on us. It happens in unexpected or unplanned circumstances.
That is, unless we are practiced in dealing with it and have made a total
commitment.

That passing acquaintance had a lasting impact on
my life. After returning home, I returned to my previous VLC Way of Eating and
lost another 100 pounds. I was also able to completely eliminate the remaining 5mg
of Micronase, a sulfonylurea
drug that I was then still taking. And my blood pressure dropped further to
110/70 (on the same meds. I was still taking a minimum dose (500mg once a day)
of Metformin. Metformin has since
become the first line of defense
in the U.S. (after “lifestyle modifications”) for Pre-diabetics and diagnosed
Type 2s.

Sulfonylurea drugs accelerate the destruction of
pancreatic beta cells. That’s why they have, in some places, fallen into
disfavor. They deplete the pancreas’s secretionary power and are one of the
reasons why Type 2 diabetes is described in the medical lexicon as a
“progressive disease.” It’s the
medical treatment that (in part) drives the progressivity. Of course,
the other equally egregious reason is
that the medical establishment still advocates
a “balanced diet,” instead of restricting carbs, to cope with a disease that is
defined by carbohydrate intolerance.

The sulfonylurea drugs are harmful because they
force an already seriously compromised
pancreas to secrete more insulin to deal with elevated blood glucose
from the carbs we eat. Dr. Ralph A. DeFronzo, winner of the ADA’s 2008 Banting
Medal for Scientific Achievement, stated that “beta cell failure begins earlier
and is more severe than previously thought.” Based on this finding, he argues
for “the need for early and aggressive treatment to preserve remaining beta
cell function and to limit further disease progression.”

Dr. DeFronzo’s very technical paper, later
published by the ADA, is available for free with full text and figures on PubMed.
Early in it, under the sub-heading “Prediabetes”, Dr. DeFronzo said, “In
summary, individuals with IGT [impaired glucose tolerance] are maximally or
near- maximally insulin resistant, they have lost 80% of their β-cell function,
and they have an approximate 10% incidence of diabetic retinopathy. By both
pathophysiological and clinical standpoints, these pre-diabetic individuals
with IGT should be considered to have type 2 diabetes.”

Denial is a touchy subject. It is touchy because
it is very personal. Addressing it requires the ability to look at oneself in
an objective way. That confrontation can be pretty messy if our lives are
complicated. We all have family and friends who care about us but who do not
know about the advances in understanding the optimal way to treat people whose damaged metabolisms cannot tolerate
dietary carbohydrates. To the extent practicable, the optimal way is to
not eat carbohydrates. That
course of treatment works for everybody
who has insulin resistance, is Pre-diabetic, or has been diagnosed with Type 2
diabetes. It is also a great way for anybody
to lose weight. Take an honest look at your own life, and ask yourself if you are in denial. Then, ask yourself, are
you ready to change, now?

Denial is not a river in Egypt. This blunt
pronouncement may be said by a close friend/counselor, or even an enlightened
physician, to not so gently make a
point about the need to confront a matter. In fact, it could be said to affect
a change that may be life altering. It was that way for me once. I remember it
well.

Monday, May 27, 2019

I have had a raised consciousness about food and
feeding since I began writing this blog. And one of the things I have observed
is when I feel hungry. Of course, hunger is not an emotion; it is a
physiological signal that has been sent and received that motivates us to eat.
The signal travels from our stomach, where the hormone ghrelin senses it is
empty, via the vegus nerve to the hypothalamus in the center of the brain. That
is the central place where hunger signals are interpreted and controlled. It’s
from there that the signal is sent. And we act. We eat.

The “empty stomach” message works well whether
you have a normal glucose metabolism or a disregulated glucose metabolism like
so many of us have developed. It has become disregulated because, as recommended
by our government, for most of our lifetime we have eaten the Standard American
Diet (SAD, ironically). According to the Nutrition Facts Panel on boxes and
bags of food products, that diet is 60% carbohydrate, 10% protein and 30% fat.
That’s 300g (1,200kcal) of carbohydrate, 50g (200kcal) of protein, and 66.6g
(600kcal) of fat. Total: 2,000kcal.

It’s 60% carbohydrate in part because the
government wants us to reduce the fat in our diet. So, what are you supposed to
do? Your only choices are to increase carbs or protein. And if you eschew
animal products, to avoid saturated
fat and cholesterol, as Big Brother
would have you do, what can you eat? More carbs, of course.

To feed the disregulated metabolism our
contemporary lifestyle offers us lots of packaged, pre-processed, and easily
digested “food” to choose from, most of which are carbs. We eat them, we digest
them quickly, we get quick energy, and then as they quickly empty from the
stomach, we get the “hungry again” signal. That’s why carb eaters and
especially carb addicts are always hungry. That’s why many diets recommend
between meal snacks, or even 5 or 6 “small meals” a day. If you have done these
diets, you know it is because you are
hungry. Now you know why.

So, why amI not hungry? I eat a
restricted calorie diet that is very
low carb. Most of the time I think I am in a mild state of ketosis. That allows
my body to burn fat instead of “sugar” (glucose) for energy. Stored energy, my
body fat, is my targeted fuel source. That’s why I need to eat a restricted carb and a restricted calorie diet. I need
to be in negative calorie balance
to lose weight. I am doing this without
hunger and – take note – without exercise.

I am not hungry at breakfast because, allowing a
few hours for digestion, my body has been in a mild ketogenic state for maybe
10 of the 14 hours since I last had a meal or anything to eat. That means I didn’t eat a bed-time snack. When I
am in ketosis, my body is happily
burning fat for energy. It doesn’t need ‘sugar’ (glucose) for fuel, so
it doesn’t send a hunger signal to the brain. This is a natural state, called
ketosis.

But, if I eat a breakfast anyway, I eat a
small ketogenic meal: fried
eggs, bacon and a cup of coffee with full cream and stevia powder. After that
small meal I can easily go ‘till late in the day without hunger because I am still in ketosis. But again,
mostly for cultural reasons, for lunch
I eat a very small meal of zero carbs:
just protein and fat, usually a can of sardines in water (with added salt), or
a can of kippered herring, and iced tea –and I stay in ketosis.

Then, an hour or so before supper, I sometimes sit
down to watch the news and snack
on radishes with salt and a “schmeer” of ghee or butter. At other times, I’ll
snack on celery and anchovy paste. The idea is to eat just a little fat to satiate,
or bulk to distend the stomach, to short circuit a tendency to eat too much supper.

I always used to eat too much at the evening meal. Again, I think
it was a cultural thing. For most Americans, dinner is the big meal of the day,
and cultural habits require a conscious effort to break. Dinner has always been
a big problem for me. My wife put too much on my plate (Sorry, Honey), and I
always ate it all. (I can’t blame her for that!) We learned as kids not to
leave food on the plate. (Blame it on our parents instead.) Now, with my wife’s
help (Thanks, Honey!) I am eating a small
supper, and I am passing up 2nds (even with really “palatable” food, as it
always is). We have a vast choice of menu options: fatty meats, poultry, and
seafood (fin fish and crustaceans), plus a low-carb vegetable roasted in olive
oil or finished with lots of butter. In other words, another small ketogenic
meal. This makes losing weight easy. I’m burning body fat for
energy balance.And that’s why I’m never hungry.

Sunday, May 26, 2019

What’s wrong with taking nourishment in liquid
form? It’s certainly convenient, and if you make your own “smoothie” or some
nutrient-dense concoction in a juicer or blender, you are assured of a
“healthy” beverage of your own composition and making, right? Well, “yes” up to
a point, but “no” for a host of other, very good reasons.

1)The
calories we drink go quickly “down the hatch” No chewing required. Chewing is
the first mechanical step in digestion. It takes energy and time to chew. It
also takes time for needed enzymes in the mouth, stomach and small intestine to
process chewed solid food into chyme to break it down to where it can be
absorbed. If food has already been liquefied, these physiological functions are
“side-stepped,” and calories are absorbed more quickly and easily. The order of
gastric (stomach) emptying is: liquids first, then carbs, then protein, and
then fat and fiber.

2) “The
mechanisms controlling hunger and thirst are completely different,” wrote food
writer and nutritionist Katherine Tallmadge in a December 2004 Washington Post article.
“Physiologically, your thirst is quenched once your blood and cell volume are
increased by water. This sends signals to your brain that you are no longer thirsty. In contrast, hunger is
regulated in your stomach and intestines. The hormone Ghrelin secreted in the
stomach wall helps you feel full.” Ghrelin doesn’t work as well with liquids as
it does with solid foods. “Our bodies don’t detect the calories in these liquid
foods the same way as when we eat solid foods,” Tallmadge said.

3)Liquid
calories add up in a way that can be surprising. The liquid calories in
smoothies, juice drinks, sodas and even specialty coffees are stealthy. “A
White Chocolate Mocha totals 410 calories (whole milk, no whip) or 510 calories
with whip. In my world, 510 calories is an entire meal,” says Elaine Magee on WebMD. Tallmadge, in her
Washington Post article, concurs: “When you consider that an appropriately
sized meal is anywhere from 400 to 700 calories, and one 44-ounce Super Big
Gulp is 800 calories, you understand the scope of the problem. A 16-ounce
Starbucks blended coffee Frappuccino is 470 calories. A single mixed drink can
set you back 300 calories. One glass of wine contains at least 100 calories. “Most
caloric drinks consumed before or during a meal are not satiating and have
little effect on how much you eat in one sitting or over the course of several
meals.”

The good news,
Tallmadge notes, is that “since liquid calories don’t contribute to feelings of
satiety, cutting back on them doesn’t make people feel deprived; most find the
change is an easy one to make.” So, what changes should be considered? The
Harvard School of Public Health pondered this question and put together a
Beverage Guidance Panel. From the March 2006 issue of the American Journal of
Clinical Nutrition, here are their recommendations:

1) Water:
Quelle surprise! But pure H2O
does provide “everything the body needs – to restore fluids lost through
metabolism, breathing, sweating, and the removal of waste. It’s the perfect
beverage for quenching thirst and rehydrating your system” according to the
group. We could end this list here! We used to, come to think of it.

2) Tea
and Coffee: “Drunk plain, they are calorie-free beverages brimming with antioxidants,
flavonoids, and other biologically active substances that may be food for
health.” They especially like the strong green tea varieties served in Japan. However,
adding cream, sugar, whipped cream and flavorings make it “closer to a
dessert.”

3) Low-fat
and skim milk and soy beverages: Here’s where the Harvard School of Public
Health/Beverage Guidance Panel and I part company. I avoid the carbs in milk and
only take heavy cream. I do not avoid saturated fat, and
I do
avoid soy products altogether: e.g., soy bean oil, soy milk. But I do
use naturally fermented soy sauce.

4) Noncalorically
Sweetened Beverages: This category includes the “so-called diet sodas and
other diet drinks that are sweetened with calorie-free artificial sweeteners.
They include stevia in this category, and liquid sugar alcohols.

We have two house cats; one is
fat and one is skinny. They were both born to feral moms about 4 years ago, one
behind a pizza parlor and the other in a backyard. A non-profit trapped the
moms as part of their TNR (Trap/Neuter/Return) program. The moms were spayed,
treated and released. The offspring were also trapped or rounded up. We
fostered the last one from each litter and eventually adopted both.

Both house cats seem to like
both foods equally. They clean their dishes and put a big dent in the chow bowl
daily. They also snack at an outdoor station where we feed our own small feral
colony. That’s how we originally got involved with the local TNR non-profit. A
litter of 4 adolescent ferals walked into our
backyard about 14 years ago. They were way too old to socialize, so we fed and
eventually trapped and TNR’d them all.

The food we give the ferals is
the same Cat Chow (32% pro; 13% fat; 42% carbs), plus 2-13.5oz cans of Purina’s
“Friskies.” The analysis of these 366kcal cans is again 11% protein, but 2.5%
fat, and 27% carbs (dry matter basis). The ferals (and our house cats) also
like these offerings equally, scarfing both down twice a day. Both the house
cats and the ferals “know” each other and frequently eat side by side at the
outdoor stations.

(As an aside, one of the ferals
occasionally comes into the house, through a door left open in warm weather,
and crosses to the kitchen to eat at the house cats’ station. But never, in the
14 years that we have faithfully fed them all, have any of the ferals ever
allowed either of us to touch any of them, oreven get close.)

All the ferals are lean. So why,
given the way they are fed, is one of our house cats lean and the other fat?
They both have access to all 3 types of food. Both have good appetites, and
both have equal opportunities for exercise. Both run around the house and yard,
frequently chasing each other or birds or butterflies. The big, lean male, is
less active – more of a couch potato, but the fat female is completely
undeterred by her girth.

If this were simply a comparison
between two carnivores – our house cats – eating a high carbohydrate diet, one
could hypothesize that the “pizza baby’s” genetic makeup was epigenetically
“expressed” when she was exposed to the high-carb Fancy Feast and Friskies
diet. Or, that the “pizza baby’s” momalready had those “expressed” genes (she
survived by living behind the pizza parlor) andpassed them on to her offspringwho
were thus born predisposed and are therefore likely to get fat on a high-carb
diet. And our lean house cat – the “backyard baby” – was perhaps the
product of a feral mom who hunted mice and voles and had a different set of
genes or similar genes that had not
been epigenetically expressed by what she
ate. She therefore produced a large, well-shaped, lean male kitten. For
further reading, see Dr. Cate Shanahan’s book, “Deep Nutrition.”

Restating the question: Why
didn’t the young ferals who wandered into our backyard 14 years ago get fat on
our nutritionally poor diet? Is it because they were offspring of a carnivorous
mom who ate animal protein and fat and had not
had her genes “expressed”? Is that
why her offspring aren’t fat cats like our “pizza baby”?

We’ll
never know. Our cats will never reproduce. But how about you and your
offspring? We’re said to be omnivores,
but I would say that humans, while not obligate carnivores, are perhaps
facultative carnivores, a species that “does best on a carnivorous diet, but can
survive-but-not-thrive on a non-carnivorous one.” This has been amply
demonstrated, I think, by the effects that the high carbohydrate diet that we’ve been eating since the dawn of the
Neolithic Age, made worse recently by the highly processed industrial foods we
now eat.

Saturday, May 25, 2019

“Natural History of Type 2 Diabetes” is a heading
in a paper by Ralph A. DeFronzo, MD. Dr. DeFronzo is using the medical phrase
“natural history” to describe the progression of a disease from incidence to
diagnosis.

The paper was published in the American Diabetes
Association’s magazine, Diabetes,
after he presented the Banting award lecture at the ADA’s 2008 annual meeting in
San Francisco. This paper caught my attention for a statement Dr. DeFronzo made
about Pre-diabetes: “In summary, individuals with IGT [impaired glucose
tolerance] are maximally or near-maximally insulin resistant, they have lost 80% of their β-cell function,
and they have an approximate 10% incidence of diabetic retinopathy. By both
pathophysiological and clinical standpoints, these pre-diabetic individuals with IGT should be considered to have
Type 2 diabetes” (emphasis mine).

The takeaway from this is Dr. DeFronzo’s main point:
We need a “new paradigm” of early intervention: “The clinical implications of
these findings for the treatment of Type 2 diabetes are that the physician [my emphasis] must
intervene early, at the stage of IGT [impaired glucose tolerance] or IFG
[impaired fasting glucose].”

I am writing this blog primarily for patients in the hope that they will see the need to
“intervene early” as well. It is so much easier to control your blood sugar if
you have maximal insulin sensitivity and remaining beta cell function.

DeFronzo begins, “Individuals destined to develop
Type 2 diabetes inherit a set of genes from their parents that make their
tissues resistant to insulin” “In liver,
the insulin resistance is manifested by an overproduction of glucose during the
basal state despite the presence of fasting hyperinsulinemia and an impaired
suppression of hepatic glucose production in response to insulin, as occurs following
a meal.” (Translation: The liver overproduces glucose while we are fasting
despite low blood insulin levels.
That is why physicians now prescribe Metformin
first to both suppress this unwanted glucose production -- called gluconeogenesis
– and improve insulin sensitivity.)

“In muscle, the insulin resistance is manifest(ed)
by impaired glucose uptake following ingestion of a carbohydrate meal and
results in postprandial hyperglycemia.” “Both obesity and decreased physical
activity are insulin resistant states and, when added to the genetic burden of
insulin resistance, place a major stress on the pancreatic β-cells to augment their
secretion of insulin to offset the defect in insulin action.” (Translation:
insulin production increases to deal with both elevated levels of circulating
glucose and our impaired insulin action due to insulin resistance.)

And here’s the crux of it: “As long as the
β-cells are able to augment their secretion of insulin sufficiently to offset
the insulin resistance, glucose tolerance remains normal.” (We have two faulty mechanisms at work
here yet our blood glucose levels in response to both fed and fasting states
are still NORMAL.) “However,
with time the β-cells begin to fail and initially the postprandial plasma
glucose levels and subsequently the fasting plasma glucose concentration begins
to rise, leading to the onset of overt diabetes.” (Note: postprandial blood
sugars rise first, then laterfasting blood glucose.) That is the reason that the A1c test
has replaced the fasting blood glucose test. The A1c test measures the
average of all blood glucose values over a 3-month period and thus captures the elevated postprandial values in the
average. Ask your doctor to do an A1c test. Medicare pays for 4 tests per
year.)

“Collectively, the insulin resistance in muscle
and liver and β-cell failure have been referred to as the triumvirate.” “The
resultant hyperglycemia [elevated blood glucose] and poor metabolic control may
cause further decline in insulin sensitivity, but it is the progressive β-cell
failure that determines the rate of disease progression.”

Dr. DeFronzo’s paper
then continues to describe his own research into the β-cell failure rate in
detail but let this suffice: “Although the plasma insulin response to the
development of insulin resistance typically is increased during the natural
history of Type 2 diabetes, this does
not mean that the β-cell is functioning normally. To the contrary,
recent studies from our group have demonstrated that the onset of β-cell failure occurs much earlier and is more
severe than previously appreciated.” That frightening statement is in
plain English. I don’t think it requires any translation or interpretation on
my part. We (doctors and patients) need a “new paradigm”
of early intervention.

Friday, May 24, 2019

With the meteoric rise in the incidence of Type 2
Diabetes and obesity (“diabesity”, a cool conjunction), and their associated
public health implications, the “dreaded complications” of the pandemic should
now be front-and-center in the news. They do deserve our attention. They are
pretty scary, and fear is a good motivator.

Here’s a
truthful note from
the American Diabetes Association: “Diabetes
increases your risk for many serious health problems. The good news? With the
correct treatment and recommended lifestyle changes, many people with diabetes
are able to prevent or delay the onset of complications.” This would actually be
a gross understatement, except
for their use of the word “recommended.” Their “recommended” changes won’t
work.

I
would say that a Type 2 who follows a Very
Low Carbohydrate diet can avoid the
complications altogether. However, if you do not control your blood
sugar by diet or other means, the NIH’s Medline Plus site tells us: “If you
have diabetes, your blood sugar levels are too high. Over time, this can
cause problems with other body functions, such as your kidneys, nerves,
feet, and eyes. Having diabetes can also put you at a
higher risk for heart disease [and] skin problems, digestive problems, sexual
dysfunction, and problems with your teeth and gums.”

The
order of magnitude of the risks of complications of chronic Type 2 diabetes are
described in a Wikipedia entry:“In the developed
world, diabetes is the most
significant cause of adult blindness in the non-elderly and the leading cause of non-traumatic
amputation in adults, and diabetic
nephropathy is the main illness
requiring renal
dialysis in the
United States” (emphases all mine). All
of these complications are directly associated with Type 2 diabetes, and they
are all the result of damage
to the small blood vessels. These complications are all described as microvascular.

In
addition, Diabetic encephalopathy, the increased cognitive decline and risk of
dementia – including Alzheimer’s disease – is observed in and associated with
chronically elevated blood sugar, i. e. inadequately controlled Type 2
diabetes. These are just some
of the risks, but I said I wasn’t going to scare the bejesus out of you. I
guess I lied.

An abstract
presented at a poster session at a 2012 ADA meeting is apt. It reported a
Swedish observational study of 12,359 patients with poorly controlled Type 2 diabetes.
None of the patients had any cardiovascular or coronary heart disease at
baseline. The patients averaged 62 years of age with mean disease duration of 9
years. The average baseline A1cwas 7.8% and their mean body mass
index was 30. Their mean blood pressure was 140/78. 62% were taking
antihypertensive (blood pressure) meds and 46% were on lipid-lowering
(cholesterol) drugs.

After 5 years,
the study’s investigators separated the patients into 2 groups: those whose A1c
decreased by at least 1% over the 5 years (6,841) and those whose A1c remained
stable or increased (5,518). At the study’s conclusion the mean A1c was 7% in
the improved-control group (-0.8%) and 8.4% in the poorly controlled group
(+0.7%). By then, 12% of the well-controlled group and 20% of the poorly
controlled group had developed coronary heart disease (CHD). Cardiovascular
disease (CVD) was present in 17% of those in the well-controlled group and 30%
of the poorly controlled group. And all-cause mortality was 15% among the group
with no improvement in A1c and 10% in the group with improved A1c. Thus, after
adjusting for baseline risk factors during the study period, they concluded that
“patients who had suboptimal glycemic
control and reduced their A1c value by slightly less that 1% were 50% less
likely to die within 5 years than were patients whose A1c did not improve.”
Wow! A1c down <1%.

So, with an
improvement in A1c of less than 1% (7.8 to 7.0%), there is still a 50% benefit.
I wonder what the benefit would be for a 2% improvement in A1c? Would the increased risk of cardiovascular
disease, coronary heart disease, and all-cause mortality be eliminated
completely? That’s something you might want to think about.

Thursday, May 23, 2019

Fructose is commonly thought to be “fruit sugar.”
And fruit is generally thought of as a “healthy” food, since it is “natural” (although
hybridized to be made sweeter). It has fiber, pectin, micronutrients and
phytochemicals, all of whose mysteries we have yet to unwrap. Still, we
consider them all beneficial. As a result, there is a widely held perception that
since all fruit contains “natural sugars,” it is therefore okay to eat whole
fruit in moderation. Besides, who can eat a dozen apples? True enough, except:
watch out for apple sauce and apple juice. These two highly processed apple food
products are very high in liquefied
sugars and especially high in fructose.
Pears too.

But fructose, the “natural fruit sugar,” is not
just found in fruit. It is present naturally in many other whole foods. Fructose
is 40% to 67% of the sugar in fruits, from 38% to 55% of the sugars in some
vegetables, and 49% to 82% of the sugar in sweeteners, both natural and
manufactured. Fructose is 50% of the content of granulated sugar, made
either from sugar caneor sugar beets. And fructose is 55%
of the liquid form of high fructose corn syrup (HFCS) used to sweeten
soft drinks in the U.S. HFCS is also used for a variety of other reasons in
solid foods, including “mouth feel.” In a loaf of bread, it is brushed on the
surface to brown it when baked and to get those whole grains to stick. The HFCS
used in baked goods and many more products is a special type that is only 42%
fructose.

The table
below, created from USDA and Wiki sources, lists common “foods,” including
fruits, vegetables and sweeteners (natural, refined and manufactured). It is
sorted by total percent fructose.

Sugars
in Foods

Sucrose

Free

Free

Other

Total

Total

Fructose/

as
% of total sugars

50%F/50%G

Fructose

Glucose

Sugars

Fructose

Glucose

glucose ratio

agave
nectar

0%

82%

18%

0

82%

18%

4.47

pear

8%

63%

29%

0

67%

33%

2.06

apple

20%

57%

23%

0

67%

33%

2.01

water
melon

20%

55%

26%

0.06

64%

36%

1.81

HFCS55
(beverages)

0%

55%

41%

4%

57%

43%

1.34

sweet
red pepper

0%

55%

45%

0

55%

45%

1.21

honey

1%

53%

46%

4.54

53%

47%

1.14

grapes

1%

52%

46%

0

53%

47%

1.12

pineapple

61%

21%

17%

0

52%

48%

1.09

molasses

54%

24%

22%

0

51%

49%

1.03

Granulated
sugar

100%

0%

0%

0%

50%

50%

1.00

beet
sugar

100%

0%

0%

0%

50%

50%

1.00

brown
sugar

97%

1%

1%

1%

50%

50%

1.00

red
beet

97%

1%

1%

0

50%

50%

1.00

carrot

75%

13%

13%

0

50%

50%

1.00

popcorn

69%

16%

16%

0

50%

50%

1.00

banana

20%

40%

41%

0

50%

50%

0.98

maple
syrup

96%

1%

3%

0

49%

51%

0.96

dried
fig

0%

48%

52%

0

48%

52%

0.92

sweet
onion

14%

40%

46%

0

47%

53%

0.89

peach

58%

18%

24%

0

47%

53%

0.89

sweet
potato

60%

17%

24%

0

46%

54%

0.87

HFCS42
(solid foods)

0%

42%

53%

5%

44%

56%

0.79

apricot

64%

10%

26%

0

42%

58%

0.72

plum

16%

32%

52%

0

40%

60%

0.66

sweet
corn

15%

31%

55%

0

38%

62%

0.61

After agave nectar (82% fructose), pears and
apples are the worst (2/3rds fructose). And natural sweeteners like honey and
maple syrup are about half fructose, and they aren’t even fruit! Only corn is low,
but higher in glucose.

About Me

I was diagnosed a Type 2 diabetic in 1986. I started a Very Low Carb diet (Atkins Induction) in 2002 to lose weight. I didn’t realize at the time that it would put my diabetes in clinical remission, or that I would be able to give up almost all of my oral diabetes meds. I also didn’t understand that, as I lost weight and continued to eat Very Low Carb, my blood lipids would dramatically improve (doubling my HDL and cutting my triglycerides by 2/3rds) and that my blood pressure would drop from 130/90 to 110/70 on the same meds.
Over the years I changed from Atkins to the Bernstein Diet (designed for diabetics) and, altogether lost 170 pounds. I later regained some and then lost some. As long as I eat Very Low Carb, I am not hungry and I have lots of energy. And I no longer have any of the indications of Metabolic Syndrome.
My goal, as long as I have excess body fat, is to remain continuously in a ketogenic state, both for blood glucose regulation and continued weight loss. I expect that this regimen will continue to provide the benefits of reduced systemic inflammation, improved blood lipids and lower blood pressure as well.